Department of Non-communicable Disease Epidemiology, Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, Keppel Street, London, WC1E 7HT, UK.
Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø and Department of Neurology, University Hospital of North Norway, 9037, Tromsø, Norway.
BMC Cardiovasc Disord. 2020 Mar 17;20(1):138. doi: 10.1186/s12872-020-01417-0.
Few reports are available on the contribution of general and abdominal obesity to the progression of carotid atherosclerosis in late adulthood. This study investigated the impact of four simple anthropometric measures of general and abdominal obesity on the progression of carotid atherosclerosis and the extent to which the association between adiposity and the progression of plaque burden is mediated by cardiometabolic markers.
Four thousand three hundred forty-five adults (median age 60) from the population-based Tromsø Study were followed over 7 years from the first carotid ultrasound screening to the next. The progression of carotid atherosclerosis was measured in three ways: incidence of plaques in previously plaque-free participants; change in the number of plaques; and total plaque area (TPA). We used generalised linear models to investigate the association between each adiposity measure - body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) - and each outcome. Models were adjusted for potential confounders (age, sex, smoking, education, physical activity). The pathways through which any associations observed might operate were investigated by further adjusting for cardiometabolic mediators (systolic blood pressure, cholesterol, and HbA1c).
There was little evidence that adiposity was related to the formation of new plaques during follow-up. However, abdominal adiposity was associated with TPA progression. WHtR showed the largest effect size (mean change in TPA per one standard deviation (SD) increase in WHtR of 0.665 mm, 95% confidence interval 0.198, 1.133) while BMI showed the smallest. Effect sizes were substantially reduced after the adjustment for potential mediators.
Abdominal obesity indirectly measured with WC seems more strongly associated with the progression of TPA than general obesity. These associations appear to be largely mediated by known cardiometabolic markers.
关于一般和腹部肥胖对成年后期颈动脉粥样硬化进展的影响，仅有少数报告。本研究调查了四种简单的一般和腹部肥胖人体测量指标对颈动脉粥样硬化进展的影响，以及肥胖与斑块负担进展之间的关联在多大程度上受到代谢指标的影响。
4345 名成年人（中位年龄 60 岁）来自基于人群的特罗姆瑟研究，从第一次颈动脉超声筛查到下一次筛查，随访 7 年。颈动脉粥样硬化的进展通过三种方式测量：在以前无斑块的参与者中斑块的发生率；斑块数量的变化；总斑块面积（TPA）。我们使用广义线性模型来研究每个肥胖指标（体重指数（BMI）、腰围（WC）、腰臀比（WHR）和腰围身高比（WHtR））与每种结果之间的关系。模型调整了潜在混杂因素（年龄、性别、吸烟、教育、体力活动）。通过进一步调整代谢指标（收缩压、胆固醇和 HbA1c），研究了观察到的任何关联可能通过的途径。
肥胖与随访期间新斑块形成之间几乎没有关系。然而，腹部肥胖与 TPA 进展有关。WHtR 显示出最大的效应大小（WHtR 每增加一个标准差（SD），TPA 的平均变化为 0.665mm，95%置信区间为 0.198，1.133），而 BMI 显示的效应最小。在调整潜在介质后，效应大小大大降低。
用 WC 间接测量的腹部肥胖与 TPA 的进展似乎比一般肥胖更密切相关。这些关联似乎主要由已知的代谢指标介导。
